Identification of EML4 as a key hub gene for endometriosis and its molecular mechanism and potential drug prediction based on the GEO database

XIANBAO FANG, MINGYAN TANG, ZIYANG YU, JIAQI DING, CHONG CUI, Hong Zhang
In: BIOCELL · 2023 · vol. 47(9) , pp. 2059–2068 · doi:10.32604/biocell.2023.030565 · W4385845565
article OA: diamond CC0
🔓 Open OA copy View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This bioinformatics study identified EML4 as a key upregulated gene in endometriosis, associated with immune cell infiltration, and predicted DB05104 (asimadoline) as a potential EML4 inhibitor.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This bioinformatics study used GEO gene expression profiles to compare endometriosis samples versus healthy controls, identifying differentially expressed genes with limma and focusing on echinoderm microtubule-associated protein-like 4 (EML4) for pathway and regulatory analyses. With Spearman correlation and GSVA enrichment, EML4 was significantly upregulated in endometriosis and correlated with 30 pathways, including glycosaminoglycan and glycosphingolipid biosynthesis pathways, while ESTIMATE-based immune correlation analyses found immune-related pathway differences between endometriosis and normal samples. The study further reported associations of EML4 with multiple immune cell types and states in endometriosis, and used Swiss-Model plus docking/dynamics approaches to predict five potential EML4 inhibitors, highlighting DB05104 (asimadoline) as a compound that bound well and was modeled to affect EML4 activity. A key limitation is that the work relies on computational analyses of a small set of GEO samples (10 cases, 10 controls) rather than experimental validation. This paper is centrally about endometriosis — it identifies EML4 as a hub gene, links it to immune-related pathways, and predicts potential EML4-targeting inhibitors.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Objective: Key genes were screened to analyze molecular mechanisms and their drug targets of endometriosis by applying a bioinformatics approach. Methods: Gene expression profiles of endometriosis and healthy controls were obtained from the Gene Expression Omnibus database. Significant differentially expressed genes were screened using the limma package. Correlation pathways were screened by Spearman correlation analysis on the echinoderm microtubule-associated protein-like 4 (EML4) and enrichment in endometriosis pathways and estimated by the GSVA package. Immune characteristics were assessed by the “ESTIMATE” R package. Potential regulatory pathways were determined by enrichment analysis. The SWISS-MODE website was used in homology modeling with EML4 and EML4 protein activity was predicted. VarElect was employed in molecular docking for screening potential compound inhibitors targeting endometriosis. Results: Ten endometriosis and 10 normal samples were included. EML4 was significantly upregulated in endometriosis (p < 0.05). Thirty significantly correlated pathways involving 18 positive and 12 negative correlations, including GLYCOSAMINOGLYCAN_BIOSYNTHESIS_HEPARAN_SULFATE and GLYCOSPHINGOLIPID_BIOSYNTHESIS_GANGLIO_SERIES were screened between EML4 and endometriosis. Immunocorrelation analysis showed a significant difference in immune-related pathways in endometriosis and normal samples (p < 0.05). In endometriosis, EML4 was associated with T-cell CD4 resting memory, activated mast cells, plasma cells, activated NK cells, M2 macrophages, and follicular helper T cells (p < 0.05). Molecular docking identified five potential inhibitors of EML4, and compound DB05104 (asimadoline) bound well to EML4 protein to exert its physiological effects. Conclusion: Differential gene expression and immune correlation analyses revealed that EML4 may affect endometriosis through multiple targets and pathways, the mechanism of which involved immune cell activation and infiltration. Molecular docking and dynamics simulation verified DB05104 as a potential inhibitor of EML4 and a powerful target for endometriosis treatment.

My notes (saved in your browser only)

Condition tags

endometriosis

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (36)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK